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Division of Endocrinology, Veterans Affairs Medical Center, Long Beach, Long Beach, California 90822; and Departments of Medicine, Biochemistry, and Pharmacology, University of California, Irvine, Irvine, California 92717
Address all correspondence and requests for reprints to: Ellis R. Levin M.D., Medical Service (11/111-I) Long Beach Veterans Affairs Medical Center, 5901 East 7th Street, Long Beach, California. E-mail: ellis.levin{at}med.va.gov.
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ABSTRACT |
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INTRODUCTION |
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and ERß have been demonstrated (reviewed in Ref. 2), and the receptors have similar affinity for steroid ligand. Estrogen binding to nuclear receptors activates or represses gene transcription, resulting from the steroid-receptor complex binding to DNA at estrogen response elements in the promoters of target genes. A second, nonclassical mechanism involves the interaction of nuclear estradiol (E2)/ER with transcription factors, such as activator protein 1 (AP-1) or Sp-1, that in turn bind their cognate DNA elements (3). This leads to alteration of chromatin, histone unwinding, and interactions with components of the basal transcription machinery complex. In both scenarios, recruitment of coactivators (and displacement of corepressors) to the sites of DNA binding modulates gene and subsequent protein expression. In addition, steroid actions occur at the cell surface, a function that is conserved from plants to humans (2, 4, 5). It is widely appreciated that membrane ER signaling through kinase cascades, calcium, and other second messengers impacts transcription (6, 7). For instance, E2 stimulation of the cyclin D1 gene occurs through ERK or phosphatidylinositol 3-kinase (PI3K) activation, promoting G1/S cell cycle progression in breast cancer cells expressing endogenous ERs (8). Many sex steroid effects reflect the integration of actions at several receptor pools. Work over the past decade has identified important mechanisms whereby membrane-initiated signaling through growth factor receptors or membrane ERs impacts the function of nuclear ERs, as one model. Integrative signaling by E2 from several sites in the cell results both in rapid and prolonged actions, and provides plasticity for the cell response to the sex steroid.
In this review, I highlight the recent developments in understanding the nature of the membrane ER, and the emerging field of integration of membrane and nuclear receptor signaling. Applications of these mechanisms to physiological and pathophysiological models of estrogen action are emphasized, and new concepts of receptor cross-talk for both genomic and nongenomic actions are identified.
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MEMBRANE ER |
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(10), and the codetection of membrane and nuclear ERs after nuclear ER cDNA expression in ER null cells (11). Chambliss et al. (12) have identified endogenous ER and ERß receptors of 67 and 54 kDa, respectively, in the caveolae and cell membranes from endothelial cells (ECs). This was done using antibodies against the classical nuclear ER and ERß. More recent data indicate that cells from the DERKO mouse (ER and ERß deleted) fail to show endogenous membrane or nuclear ER or ERß, by Western blot (13), E2 binding, and rapid signaling. Definitive proof that endogenous membrane and nuclear ERs are the same protein requires isolation and sequencing of the two receptor pools.
Work from the laboratory of Bender and associates (14) has reported a truncated, 46-kDa receptor as the predominant ER isoform at the plasma membrane of an immortalized human EC line. However, several other laboratories working with isolated ECs and/or aorta have not identified the 46-kDa receptor to be abundant, including at the cell membrane (12, 13, 15).
Several reports have surfaced describing endogenous membrane ERs in neurons with slightly altered receptor pharmacology (16, 17). However, these receptors have not been isolated, and whether they exist in cells from DERKO mice is unknown at present. Non-ER or ER-indirectly mediated actions of E2 have also been proposed, often based on the lack of antagonism of E2 effects by ICI182780 (18). Perhaps this results from E2 facilitating the action of membrane-acting proteins (sex hormone-binding globulin) (19) or the allosteric modulation of receptors at the cell membrane (20). The full nature and relevance of these responses are unclear.
Work from several laboratories has affirmed the ability of endogenous or expressed ERs to activate G protein-related signaling at the plasma membrane (11, 21, 22). Membrane ERs possibly exist as a cytoplasmic pool tethered to the inner face of the plasma membrane bilayer through binding to proteins such as caveolin-1 (23), in conjunction with modulator of nongenomic activity of ER (MNAR) (24), or Shc and IGF-I (25). Alternatively, evidence exists for endogenous ER within isolated caveolae vesicles shorn from the plasma membrane of ECs, as well as noncaveolar compartments of the membrane (12, 23, 26). Caveolae are typically spread throughout the cell membrane, and therefore ERs could habituate within the plasma membrane at times, like growth factor receptors. It is likely that in a dynamic fashion, both models are correct, and endogenous membrane-localized ERs also spend time in non-clathrin-coated endosomes in the cytoplasm (27).
Whether ERs span the plasma membrane or contain an extracellular ligand binding region is controversial. The membrane-impermeant estrogen conjugate, E2-BSA, has been used by many laboratories to support E2 action at membrane ERs. However, it has been reported that this compound dissociates into BSA and E2 (28), requiring filtration and careful handling of this reagent. Furthermore, BSA is well known to be taken up into caveolae in the plasma membrane (29), and therefore E2-BSA can probably access ERs in this plasma membrane raft. Thus, this compound cannot be used as definitive proof that there is externalization of a segment of ERs beyond the plasma membrane. Another approach to this issue is to carry out functional studies or immunohistochemistry with antibodies to ER (9). The presumption is that antibodies do not gain access to the cell interior and therefore identify a functional extracellular domain of ERs. However, it is not clear that cells are impermeable to the antibody intruding into the plasma membrane, and thus this reagent may suffer from the same limitations as E2-BSA.
Several reports suggest that the ability of E2 to activate G proteins is mediated through an orphan G protein-coupled receptor, GPR30. However, the pharmacology of this interaction is atypical, as 17ß-E2, equimolar 17-E2, and even ICI 182780 trigger the GPR30-related response (30). One report indicated that this interaction with GPR30 required micromolar E2, perhaps indicating an allosteric modulation with questionable physiological significance (31). Furthermore, antisense oligonucleotides to GPR30 failed to prevent E2 signaling through ERK to proliferation in breast cancer (32). A recent report from Thomas et al. (33) identified GPR30 as a low-capacity receptor for E2, one capable of supporting a modest generation of cAMP. It was undetermined whether E2-GPR30 interactions contribute to the overall signaling by E2 at the plasma membrane or the downstream physiology effects in breast cancer cells.
The endogenous membrane receptor assembles as part of a large signalsome complex that includes G proteins, receptor tyrosine kinases (EGFR, IGF-I receptor), and nonreceptor tyrosine kinases, such as Src (34). In a confined space, undetermined dynamics of signal molecule configuration lead to discrete G protein subunit activation. For instance, E2/ER coimmunoprecipitates with and activates Gs and Gq in transfected or endogenous ER cell models (11, 13), and Gi in ECs (21). G and Gß
activation lead to downstream augmentation of kinase activities, such as ERK and PI3K in both breast cancer cells and ECs. This signaling impacts the cellular actions of E2 (21, 34, 35). In some instances, the association of ER with G proteins may be indirect. E2 signaling to endothelial nitric oxide synthase (eNOS) activation in ECs may involve the striatin protein, which binds to ER, Gi, and caveolin-1 (36). This protein may help assemble and activate the eNOS-signaling cassette at the plasma membrane.
Recent work has defined motifs in the E domain of ER that are critical to membrane localization and function (37). This includes E domain (ligand-binding domain) residues that are necessary for dimerization of the endogenous membrane ER and ERß (13). Mutation of these motifs prevents both receptor dimerization and signaling through ERK, PI3K, and cAMP: loss of the former signals prevents the cell survival action of E2 in breast cancer cells (13). In contrast, signaling to eNOS activation in ER-transfected COS cells may not require membrane ER dimerization (37). Another residue, S522 of ER, is necessary for the physical association of this receptor with caveolin-1 protein, a protein the N-terminus scaffolding domain of which facilitates ER transport from the cytosol to the membrane (38). Interactions between the A/B domain of ER and Shc may also contribute to membrane localization through unclear transport mechanisms (39).
Very recent studies have identified an important modification of ER that facilitates both caveolin-1 binding and membrane localization. Marino and colleagues (40, 41) have shown that cystine 447 of transfected human ER is crucial to steroid-independent palmitoylation of the receptor. This E domain amino acid is necessary for ER to physically associate with the caveolin-1 protein and localize at the membrane. Mutation of this single amino acid or inhibition of palmitoylation with 2-Bromo-palmitate results in a significant decrease of expressed receptors at the plasma membrane, compared with wild-type ER expression. Furthermore, cystine 447-mutated ER does not support proliferative signaling through ERK and PI3K (41). Palmitoylation as a possible mechanism for membrane ER localization was also suggested from previous studies in endothelial cells (14). A partial model for membrane localization involves palmitoylation of ER to promote binding to caveolin-1 (which itself is palmitoylated). Subsequently, the membrane localization sequence of caveolin-1 (scaffolding domain) is crucial for ER transport to and localization at the membrane (38).
Other proteins may also facilitate the membrane localization of ERs, including MNAR, Shc and growth factor receptors, and striatin (21, 22, 36). Shc and striatin have been reported to interact with the A/B domain of ER (25, 36) whereas MNAR binds the E domain of the steroid receptor (24). Interestingly, A/B and C domain-deleted ER localizes to the membrane and signals to ERK, in the same manner as wild-type ER (38, 41). This is consistent with the idea that the E domain contains most of the information for both localization and function of ER at the membrane (42). Very recently, elements within the nuclear localization sequence (NLS) of ER (D domain) were reported as required for E2-induced ERK and PI3K and nitric oxide production through nitric oxide synthase (eNOS) activation in transfected COS cells (37). Although this may be specific to eNOS activation, Zhang et al. (43) previously reported that expression of an NLS-deleted ER, targeted to the cell membrane, supported ERK activation by E2. Thus the extent of the role of the NLS in membrane ER function is not clear.
Could nuclear ER also rapidly up-regulate kinase activity? As mentioned, NLS-deficient ERs have been reported to either affect or not affect rapid signaling by E2 (37, 43). When the E domain of ER or the full-length receptor is targeted to the nucleus, no rapid activation of ERK is detected (8). Instead, when either construct is targeted exclusively to the plasma membrane, multiple rapid signals are generated in response to E2 (44). Thus, the preponderance of available evidence suggests that the membrane localization of ERs is necessary for kinase activation, consistent with the localization and signaling by growth factor and typical G protein-coupled receptors.
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MEMBRANE ER CROSS-TALK TO THE NUCLEUS |
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). In breast cancer, the endogenous membrane ER cross-talks to the trans activation of the EGF, ErbB2, and IGF-I receptors (30, 45, 46). This results in downstream signaling to ERK MAPK and PI3 /AKT kinases. Important nonreceptor tyrosine kinases such as Src are also involved as intermediary steps (34). ERK and PI3K phosphorylate discrete residues of the endogenous nuclear ERs, up-regulating its transcriptional activity or stability (47, 48). In response to EGF or IGF-I, the nuclear ER can be activated in steroid ligand-independent fashion (47). As an example, kinase-induced phosphorylation of nuclear ER on serine 305 enhances cyclin D1 transcription in breast cancer (49). Activation from the membrane of PI3/AKT kinases can repress the downstream inhibitory actions of kinases. PI3K/AKT phosphorylation of glycogen synthase kinase (GSK)-3ß (50) disinhibits the repressive effect of GSK-3ß on ER serine 118 phosphorylation. This results in enhanced transcriptional action of the nuclear ER.
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Receptor phosphorylation also impacts selective ER modulator (SERM) effects. Tamoxifen has recently been reported to convert from an antagonist to an agonist in breast cancer, depending upon Ser 305 phosphorylation (54). This site can be phosphorylated by both protein kinase A (54) and p21-activated kinase 1 (49). Circulating or locally produced E2 or growth factors acting at the membrane could potentially stimulate this nuclear ER modification via protein kinase A (55) and contribute to tamoxifen resistance in women (56).
Membrane ER Signaling to Nuclear ER-Independent Functions
Activation of target gene transcription also occurs through membrane signaling, independently of nuclear ERs. ERK activation up-regulates AP-1 mediated genes (e.g. c-fos) (3, 52, 57). This results in part from serum response factor/elk-1 stimulation by E2, and in part by recruitment of nuclear ERs and coactivators to AP-1 sites on gene promoters. Similarly, PI3K activation by E2-induced signaling from the endogenous membrane ER rapidly up-regulates hundreds of genes in a target cell (58). One such E2-induced gene, cyclooxygenase-2, is regulated by signaling to nuclear factor-
B, potentially contributing to an important cell biological outcome of tumor angiogenesis (59).
The loss of inhibition produced by tumor suppressor gene mutation often underlies carcinogenesis (60). Such a role for membrane signaling can be proposed in steroid hormone-responsive cancers. PI3K/AKT inhibition of GSK-3ß function allows ß-catenin to translocate to the nucleus. ß-Catenin cooperates with TCF/Lef transcription factors to up-regulate proliferation genes, such as cyclin D1 (61), contributing to carcinogenesis. PI3K/AKT activation also leads to decreased Forkhead (FKHRL1) transcription factor function, the inhibition of which results in cell survival (60). Thus, membrane signaling to the nucleus through these and other, undiscovered pathways contributes to estrogen-induced cell proliferation and survival, essential features of tumor biology. It has been estimated that more than 500 kinases are encoded within the human genome (62). The ability of membrane ERs and/or growth factor receptor tyrosine kinases to signal through multiple kinases to the nucleus undoubtedly impacts all aspects of cellular function.
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NONTRANSCRIPTIONAL ACTIONS OF ER |
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Signaling by membrane ERs to PI3K reveals additional integrated functions in breast cancer. PI3K activation causes the phosphorylation of BAD, which is then sequestered by 14–3-3 proteins in the cytoplasm (64). Sequestration dissociates phosphorylated BAD from binding the antiapoptotic proteins, Bcl2 and Bcl-xl, which allows these proteins to maintain mitochondrial membrane integrity and prevent the release of cytochrome c and subsequent cell death. In some instances, downstream signaling by E2 to additional kinase substrates (mammalian target of rapamycin for PI3K/Akt or p70S6 kinase for AKT or ERK) is required, and these target signals expand the potential repertoire of E2 actions. For instance, the p70S6 kinase modulates protein translation and is important for sensing and responding to the nutrient status of the organism (65). The localization and duration of kinase signaling may importantly contribute to E2 actions in these respects. For instance, the ability of estrogen to rescue osteocytes or induce cell death in osteoclasts is dictated, in part, by the duration of ERK activation, and whether this kinase signals predominantly in cytoplasm or nucleus (66, 67).
E2 also promotes the motility of cells through signaling via p38 (35) and perhaps PI3K pathways (68). The latter signal activates the small GTP proteins Rac and Cdc42, which in conjunction with Rho kinase, modulate target cell migration (69). Cell motility is ultimately driven by the formation of lamellipodia and extension of filipodia, and estrogen promotes this (25). Motility depends on nucleated actin-related processes, the synthesis of capping proteins, and association of ARP 2/3 and Ena/VASP regulatory proteins with actin-barbed ends (70). These proteins are potential substrates for posttranslational modification by E2 signaling.
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ERs IN CYTOPLASM |
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CELL PHYSIOLOGY OUTCOMES OF RAPID SIGNALING BY E2 |
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TOPABSTRACTINTRODUCTIONMEMBRANE ERMEMBRANE ER CROSS-TALK TO...NONTRANSCRIPTIONAL ACTIONS OF ERERs IN CYTOPLASMCELL PHYSIOLOGY OUTCOMES OF...PERSPECTIVEREFERENCES |
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From this work, it has been proposed that estrogenic compounds that only act at the cell membrane might not stimulate the proliferation of cells, and thus not promote breast or uterine neoplasia. This concept requires rigorous demonstration, because signaling through kinase activation strongly promotes breast cancer cell proliferation in vitro and in vivo (78, 79). Developing agonists or antagonists that act strictly at membrane ERs should allow better understanding of the contributions of this receptor pool to overall E2 action and provide possible targets for therapeutic intervention.
Analogous to this, the development of newer generations of SERMS should consider whether their actions result from binding membrane and/or nuclear ERs. It has been shown that raloxifene activates the same kinase signaling pathways as E2, to trigger nitric oxide production in ECs (80, 81). This leads to enhanced cardiac perfusion and contractility of the ischemic heart in vivo (82). This is consistent with the ability of E2 to prevent ischemia-reperfusion injury in mice, via PI3K signaling from the membrane receptor (83).
Estrogenic compounds also prevent neuronal cell death, induced by cerebrovascular ischemia in vivo. Several groups have shown that E2 rescues rodents from neuronal apoptosis, in part through ER up-regulation of cell survival genes (84, 85, 86, 87). This may be related, in part, to signaling though PI3K (88, 89). E2 also prevents alcohol-induced neuronal injury by modifying protein kinase C activity (90). These results suggest that membrane ER signaling contributes to the overall neuroprotective effects of the sex steroid. In this regard, rapidly signaling ERs are localized to the neurites, and not the nuclei of neurons (91). These in vivo data have resulted in the development of estrogen compounds that protect neurons against insult-induced cell death but bind poorly to ER or ERß (87). ER-independent neuroprotective effects of estrogenic compounds during stroke may be related to the prevention of reactive oxygen species formation (92). In other work, estrogen rapidly signals to CREB phosphorylation and ERK activation in neurons. This is mediated by the classical ER ( or ß) expressed in a specific brain region, and was shown using ER knock-out mice (93).
Estrogen action certainly impacts ovarian follicle development, and this may reflect integrated functions of membrane and nuclear ERs. An important family of transcription factors in follicle development are the Forkhead proteins. In vivo and in vitro rodent models indicate that the transcription and actions of Foxo1, FKHRL1, and AFX are regulated by growth factors and estrogen and depend on kinase modulation (94). For instance, its is well recognized that PI3K/AKT phosphorylates and thus sequesters Forkhead proteins in the cytoplasm (50), thus limiting transcriptional activity. This is a pathway that E2 activates in virtually all ER-producing cell types investigated. Activation of this pathway in ovarian cancer by the sex steroid leads to increased telomerase gene expression and activity, thus contributing to tumor propagation (95). E2 activates p21-activated kinase in breast cancer cells, also leading to FKHR phosphorylation/sequestration (96). In breast cancer, hypersensitivity of estrogen-deprived cells corresponds to increased ERK activation and resulting Elk-1 transcription factor activation (97). Additional in vivo models utilizing physiological concentrations of estrogen will be necessary to define the pathophysiological roles of sex steroid signaling from the membrane to tumor promotion.
Tamoxifen resistance in breast cancer may be related to enhanced cross-talk between the membrane ER and EGFR family member receptors, most notably ErbB2 (HER-2). When ErbB2 is experimentally overexpressed, tamoxifen activates both ER and ErbB2 to signal downstream through ERK and PI3K to AIB1 phosphorylation (98). Tamoxifen acts as an agonist in this situation, promoting coactivator recruitment as a result of kinase signaling. EGFR tyrosine kinase inhibition reconverts tamoxifen to an antagonist and disassembles the positive transcription complex on the promoter of a target gene. An emerging therapeutic approach in this malignancy is estrogen purging, in which raloxifene-resistant cancer cells undergo E2-induced apoptosis (99). Thus, integrative signaling from the membrane through kinase-induced transcription, or posttranscriptional effects on protein function, contributes to the tumor-promoting actions of estrogen in vivo and may contribute to SERM resistance.
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PERSPECTIVE |
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Nevertheless, many cells divide, attempt to survive, migrate, and differentiate. These common functions allow us the opportunity to deduce cellular programs that are shared between steroid hormone-responsive cells. Such programs provide potential interventional targets to enhance or inhibit estrogen functions. Elucidating the details of these programs could provide a more informed approach to disorders resulting from reproductive organ dysfunction, the prevention of osteoporosis after the menopause, or sex steroid-responsive cancers. Estrogen-related reagents that target a particular receptor pool may be efficacious in these respects (25, 76), but we will have to better understand the integrative nature of hormonal action to avoid undesirable consequences of this approach.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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First Published Online February 10, 2005
Abbreviations: AP-1, Activator protein 1; E2, estradiol; EC, endothelial cell; ER, estrogen receptor; EGFR, epidermal growth factor receptor; eNOS, endothelial nitric oxide synthase; FKHRL1, Forkhead; GPR30, G protein-coupled receptor 30; GSK, glycogen synthase kinase; MNAR, modulator of nongenomic activity of ER; NLS, nuclear localization signal; PI3K, phosphatidylinositol 3-kinase; SERM, selective ER modulator.
Received for publication September 30, 2004. Accepted for publication February 3, 2005.
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detected on the plasma membrane of aldehyde-fixed GH3/B6/F10 rat pituitary tumor cells by enzyme-linked immunocytochemistry. Endocrinology 140:3805–3814 and ERß expressed in CHO cells. Mol Endocrinol 13:307–319 variant (ER46) in human endothelial cells. Proc Natl Acad Sci USA 100:4807–4812 may be dispensable to mediate the effect of estradiol on endothelial NO production in mice. Proc Natl Acad Sci USA 99:2205–2210(i). J Biol Chem 276:27071–27076 to the plasma membrane. Proc Natl Acad Sci USA 101:2076–2081 localized in caveolae. Biochem Biophys Res Commun 263:257–262[CrossRef][Medline]
. Proc Natl Acad Sci USA 101:17126–17131 domains with known nuclear functions. Mol Endocrinol 19:277–289. Mol Cell Biol 23:1633–1646-Shc association and Shc pathway activation. Mol Endocrinol 16:116–127 functions. Biochem Biophys Res Commun 316:878–883[CrossRef][Medline]
membrane localization regulation by 17 ß-estradiol. Mol Biol Cell 16:231–237 mediates estrogen effect on MAPK activation. Biochem Biophys Res Commun 294:926–933[CrossRef][Medline]
rapidly activates the IGF-1 receptor pathway. J Biol Chem 275:18447–18453 after PKA activation in breast cancer. Cancer Cell 5:597–605[CrossRef][Medline]
and ERß in human MCF7 cells. Am J Physiol Endocrinol Metab 286:E1011–E1022
gene expression and activity can be modulated by the ErbB2/PI 3-K/Akt pathway. Oncogene 22:7998–8011[CrossRef][Medline]
, not ß, is a critical link in estradiol-mediated protection against brain injury. Proc Natl Acad Sci USA 98:1952–1957 mediates rapid signaling by estrogen. J Neurosci Res 74:1–11[CrossRef][Medline]
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A. Pedram, M. Razandi, J. K Kim, F. O'Mahony, E. Y. Lee, U. Luderer, and E. R. Levin Developmental Phenotype of a Membrane Only Estrogen Receptor {alpha} (MOER) Mouse J. Biol. Chem., February 6, 2009; 284(6): 3488 - 3495. [Abstract] [Full Text] [PDF]
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S. Merlo, G. Frasca, P. L. Canonico, and M. A. Sortino Differential involvement of estrogen receptor{alpha} and estrogen receptor{beta} in the healing promoting effect of estrogen in human keratinocytes J. Endocrinol., February 1, 2009; 200(2): 189 - 197. [Abstract] [Full Text] [PDF]
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G. Zhang, X. Liu, A. M. Farkas, A. V. Parwani, K. L. Lathrop, D. Lenzner, S. R. Land, and H. Srinivas Estrogen Receptor {beta} Functions through Nongenomic Mechanisms in Lung Cancer Cells Mol. Endocrinol., February 1, 2009; 23(2): 146 - 156. [Abstract] [Full Text] [PDF]
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Y. Merot, F. Ferriere, L. Gailhouste, G. Huet, F. Percevault, C. Saligaut, and G. Flouriot Different Outcomes of Unliganded and Liganded Estrogen Receptor-{alpha} on Neurite Outgrowth in PC12 Cells Endocrinology, January 1, 2009; 150(1): 200 - 211. [Abstract] [Full Text] [PDF]
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F. Wu, R. Xu, K. Kim, J. Martin, and S. Safe In Vivo Profiling of Estrogen Receptor/Specificity Protein-Dependent Transactivation Endocrinology, November 1, 2008; 149(11): 5696 - 5705. [Abstract] [Full Text] [PDF]
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S. D. Conzen Minireview: Nuclear Receptors and Breast Cancer Mol. Endocrinol., October 1, 2008; 22(10): 2215 - 2228. [Abstract] [Full Text] [PDF]
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L. Hu, R. L. Gustofson, H. Feng, P. Ki Leung, N. Mores, L. Z. Krsmanovic, and K. J. Catt Converse Regulatory Functions of Estrogen Receptor-{alpha} and -{beta} Subtypes Expressed in Hypothalamic Gonadotropin-Releasing Hormone Neurons Mol. Endocrinol., October 1, 2008; 22(10): 2250 - 2259. [Abstract] [Full Text] [PDF]
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R. Sirianni, A. Chimento, C. Ruggiero, A. De Luca, R. Lappano, S. Ando, M. Maggiolini, and V. Pezzi The Novel Estrogen Receptor, G Protein-Coupled Receptor 30, Mediates the Proliferative Effects Induced by 17{beta}-Estradiol on Mouse Spermatogonial GC-1 Cell Line Endocrinology, October 1, 2008; 149(10): 5043 - 5051. [Abstract] [Full Text] [PDF]
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C. Otto, B. Rohde-Schulz, G. Schwarz, I. Fuchs, M. Klewer, D. Brittain, G. Langer, B. Bader, K. Prelle, R. Nubbemeyer, et al. G Protein-Coupled Receptor 30 Localizes to the Endoplasmic Reticulum and Is Not Activated by Estradiol Endocrinology, October 1, 2008; 149(10): 4846 - 4856. [Abstract] [Full Text] [PDF]
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C. Wang, E. R. Prossnitz, and S. K. Roy G Protein-Coupled Receptor 30 Expression Is Required for Estrogen Stimulation of Primordial Follicle Formation in the Hamster Ovary Endocrinology, September 1, 2008; 149(9): 4452 - 4461. [Abstract] [Full Text] [PDF]
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J. M. Flynn, S. D. Dimitrijevich, M. Younes, G. Skliris, L. C. Murphy, and P. R. Cammarata Role of wild-type estrogen receptor-{beta} in mitochondrial cytoprotection of cultured normal male and female human lens epithelial cells Am J Physiol Endocrinol Metab, September 1, 2008; 295(3): E637 - E647. [Abstract] [Full Text] [PDF]
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C. Glidewell-Kenney, J. Weiss, L. A. Hurley, J. E. Levine, and J. L. Jameson Estrogen Receptor {alpha} Signaling Pathways Differentially Regulate Gonadotropin Subunit Gene Expression and Serum Follicle-Stimulating Hormone in the Female Mouse Endocrinology, August 1, 2008; 149(8): 4168 - 4176. [Abstract] [Full Text] [PDF]
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L. Albanito, D. Sisci, S. Aquila, E. Brunelli, A. Vivacqua, A. Madeo, R. Lappano, D. P. Pandey, D. Picard, L. Mauro, et al. Epidermal Growth Factor Induces G Protein-Coupled Receptor 30 Expression in Estrogen Receptor-Negative Breast Cancer Cells Endocrinology, August 1, 2008; 149(8): 3799 - 3808. [Abstract] [Full Text] [PDF]
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X. Di, L. Yu, A.B. Moore, L. Castro, X. Zheng, T. Hermon, and D. Dixon A low concentration of genistein induces estrogen receptor-alpha and insulin-like growth factor-I receptor interactions and proliferation in uterine leiomyoma cells Hum. Reprod., August 1, 2008; 23(8): 1873 - 1883. [Abstract] [Full Text] [PDF]
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 C. M. Klinge, N. S. Wickramasinghe, M. M. Ivanova, and S. M. Dougherty Resveratrol stimulates nitric oxide production by increasing estrogen receptor {alpha}-Src-caveolin-1 interaction and phosphorylation in human umbilical vein endothelial cells FASEB J, July 1, 2008; 22(7): 2185 - 2197. [Abstract] [Full Text] [PDF]
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D. Titolo, C. M. Mayer, S. S. Dhillon, F. Cai, and D. D. Belsham Estrogen Facilitates both Phosphatidylinositol 3-Kinase/Akt and ERK1/2 Mitogen-Activated Protein Kinase Membrane Signaling Required for Long-Term Neuropeptide Y Transcriptional Regulation in Clonal, Immortalized Neurons J. Neurosci., June 18, 2008; 28(25): 6473 - 6482. [Abstract] [Full Text] [PDF]
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 M. Belakavadi, P. K. Pandey, R. Vijayvargia, and J. D. Fondell MED1 Phosphorylation Promotes Its Association with Mediator: Implications for Nuclear Receptor Signaling Mol. Cell. Biol., June 15, 2008; 28(12): 3932 - 3942. [Abstract] [Full Text] [PDF]
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 T. L. McCarthy, M. E. Clough, C. M. Gundberg, and M. Centrella Expression of an estrogen receptor agonist in differentiating osteoblast cultures PNAS, May 13, 2008; 105(19): 7022 - 7027. [Abstract] [Full Text] [PDF]
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P. Hu, H. K. Kinyamu, L. Wang, J. Martin, T. K. Archer, and C. Teng Estrogen Induces Estrogen-related Receptor {alpha} Gene Expression and Chromatin Structural Changes in Estrogen Receptor (ER)-positive and ER-negative Breast Cancer Cells J. Biol. Chem., March 14, 2008; 283(11): 6752 - 6763. [Abstract] [Full Text] [PDF]
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T. F.G Lucas, E. R Siu, C. A Esteves, H. P Monteiro, C. A Oliveira, C. S Porto, and M. F. M Lazari 17Beta-Estradiol Induces the Translocation of the Estrogen Receptors ESR1 and ESR2 to the Cell Membrane, MAPK3/1 Phosphorylation and Proliferation of Cultured Immature Rat Sertoli Cells Biol Reprod, January 1, 2008; 78(1): 101 - 114. [Abstract] [Full Text] [PDF]
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N. Zhu and U. Hansen HMGN1 Modulates Estrogen-Mediated Transcriptional Activation through Interactions with Specific DNA-Binding Transcription Factors Mol. Cell. Biol., December 15, 2007; 27(24): 8859 - 8873. [Abstract] [Full Text] [PDF]
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 S. R. Hammes and E. R. Levin Extranuclear Steroid Receptors: Nature and Actions Endocr. Rev., December 1, 2007; 28(7): 726 - 741. [Abstract] [Full Text] [PDF]
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K. Watashi, D. Inoue, M. Hijikata, K. Goto, H. H. Aly, and K. Shimotohno Anti-hepatitis C Virus Activity of Tamoxifen Reveals the Functional Association of Estrogen Receptor with Viral RNA Polymerase NS5B J. Biol. Chem., November 9, 2007; 282(45): 32765 - 32772. [Abstract] [Full Text] [PDF]
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R. Alzamora, L. R. Brown, and B. J. Harvey Direct Binding and Activation of Protein Kinase C Isoforms by Aldosterone and 17{beta}-Estradiol Mol. Endocrinol., November 1, 2007; 21(11): 2637 - 2650. [Abstract] [Full Text] [PDF]
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 S. Khan, F. Wu, S. Liu, Q. Wu, and S. Safe Role of specificity protein transcription factors in estrogen-induced gene expression in MCF-7 breast cancer cells J. Mol. Endocrinol., October 1, 2007; 39(4): 289 - 304. [Abstract] [Full Text] [PDF]
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B. M. Wittmann, A. Sherk, and D. P. McDonnell Definition of Functionally Important Mechanistic Differences among Selective Estrogen Receptor Down-regulators Cancer Res., October 1, 2007; 67(19): 9549 - 9560. [Abstract] [Full Text] [PDF]
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S. Masia, S. Alvarez, A. R. de Lera, and D. Barettino Rapid, Nongenomic Actions of Retinoic Acid on Phosphatidylinositol-3-Kinase Signaling Pathway Mediated by the Retinoic Acid Receptor Mol. Endocrinol., October 1, 2007; 21(10): 2391 - 2402. [Abstract] [Full Text] [PDF]
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J. Cheng, C. Zhang, and D. J. Shapiro A Functional Serine 118 Phosphorylation Site in Estrogen Receptor-{alpha} Is Required for Down-Regulation of Gene Expression by 17{beta}-Estradiol and 4-Hydroxytamoxifen Endocrinology, October 1, 2007; 148(10): 4634 - 4641. [Abstract] [Full Text] [PDF]
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T. J. Peterson, S. Karmakar, M. C. Pace, T. Gao, and C. L. Smith The Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptor (SMRT) Corepressor Is Required for Full Estrogen Receptor {alpha} Transcriptional Activity Mol. Cell. Biol., September 1, 2007; 27(17): 5933 - 5948. [Abstract] [Full Text] [PDF]
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B. T. Akingbemi, T. D. Braden, B. W. Kemppainen, K. D. Hancock, J. D. Sherrill, S. J. Cook, X. He, and J. G. Supko Exposure to Phytoestrogens in the Perinatal Period Affects Androgen Secretion by Testicular Leydig Cells in the Adult Rat Endocrinology, September 1, 2007; 148(9): 4475 - 4488. [Abstract] [Full Text] [PDF]
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A. Pedram, M. Razandi, R. C. A. Sainson, J. K. Kim, C. C. Hughes, and E. R. Levin A Conserved Mechanism for Steroid Receptor Translocation to the Plasma Membrane J. Biol. Chem., August 3, 2007; 282(31): 22278 - 22288. [Abstract] [Full Text] [PDF]
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A. Morales, M. Gonzalez, R. Marin, M. Diaz, and R. Alonso Estrogen inhibition of norepinephrine responsiveness is initiated at the plasma membrane of GnRH-producing GT1-7 cells J. Endocrinol., July 1, 2007; 194(1): 193 - 200. [Abstract] [Full Text] [PDF]
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P. Kumar, Q. Wu, K. L. Chambliss, I. S. Yuhanna, S. M. Mumby, C. Mineo, G. G. Tall, and P. W. Shaul Direct Interactions with G{alpha}i and G{beta}{gamma} Mediate Nongenomic Signaling by Estrogen Receptor {alpha} Mol. Endocrinol., June 1, 2007; 21(6): 1370 - 1380. [Abstract] [Full Text] [PDF]
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A. Zheng, A. Kallio, and P. Harkonen Tamoxifen-Induced Rapid Death of MCF-7 Breast Cancer Cells Is Mediated via Extracellularly Signal-Regulated Kinase Signaling and Can Be Abrogated by Estrogen Endocrinology, June 1, 2007; 148(6): 2764 - 2777. [Abstract] [Full Text] [PDF]
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 E. Haas, M. R. Meyer, U. Schurr, I. Bhattacharya, R. Minotti, H. H. Nguyen, A. Heigl, M. Lachat, M. Genoni, and M. Barton Differential Effects of 17{beta}-Estradiol on Function and Expression of Estrogen Receptor {alpha}, Estrogen Receptor {beta}, and GPR30 in Arteries and Veins of Patients With Atherosclerosis Hypertension, June 1, 2007; 49(6): 1358 - 1363. [Abstract] [Full Text] [PDF]
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C. Glidewell-Kenney, L. A. Hurley, L. Pfaff, J. Weiss, J. E. Levine, and J. L. Jameson Nonclassical estrogen receptor {alpha} signaling mediates negative feedback in the female mouse reproductive axis PNAS, May 8, 2007; 104(19): 8173 - 8177. [Abstract] [Full Text] [PDF]
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 M. E. Wierman and W. M. Kohrt Review Article: Vascular and Metabolic Effects of Sex Steroids: New Insights Into Clinical Trials Reproductive Sciences, May 1, 2007; 14(4): 300 - 314. [Abstract] [PDF]
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A. A. Kazi and R. D. Koos Estrogen-Induced Activation of Hypoxia-Inducible Factor-1{alpha}, Vascular Endothelial Growth Factor Expression, and Edema in the Uterus Are Mediated by the Phosphatidylinositol 3-Kinase/Akt Pathway Endocrinology, May 1, 2007; 148(5): 2363 - 2374. [Abstract] [Full Text] [PDF]
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J. C Garrido-Gracia, A. Gordon, C. Bellido, R. Aguilar, I. Barranco, Y. Millan, J. M. de las Mulas, and J. E Sanchez-Criado The integrated action of oestrogen receptor isoforms and sites with progesterone receptor in the gonadotrope modulates LH secretion: evidence from tamoxifen-treated ovariectomized rats J. Endocrinol., April 1, 2007; 193(1): 107 - 119. [Abstract] [Full Text] [PDF]
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F. A. Syed, D. G. Fraser, T. C. Spelsberg, C. J. Rosen, A. Krust, P. Chambon, J. L. Jameson, and S. Khosla Effects of Loss of Classical Estrogen Response Element Signaling on Bone in Male Mice Endocrinology, April 1, 2007; 148(4): 1902 - 1910. [Abstract] [Full Text] [PDF]
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P. Galluzzo, F. Caiazza, S. Moreno, and M. Marino Role of ER{beta} palmitoylation in the inhibition of human colon cancer cell proliferation Endocr. Relat. Cancer, March 1, 2007; 14(1): 153 - 167. [Abstract] [Full Text] [PDF]
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 M. E. Wierman Sex steroid effects at target tissues: mechanisms of action Advan Physiol Educ, March 1, 2007; 31(1): 26 - 33. [Abstract] [Full Text] [PDF]
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J. G. Greger, N. Fursov, N. Cooch, S. McLarney, L. P. Freedman, D. P. Edwards, and B. J. Cheskis Phosphorylation of MNAR Promotes Estrogen Activation of Phosphatidylinositol 3-Kinase Mol. Cell. Biol., March 1, 2007; 27(5): 1904 - 1913. [Abstract] [Full Text] [PDF]
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S. A. Hart, M. A. Snyder, T. Smejkalova, and C. S. Woolley Estrogen Mobilizes a Subset of Estrogen Receptor-{alpha}-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1 J. Neurosci., February 21, 2007; 27(8): 2102 - 2111. [Abstract] [Full Text] [PDF]
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L. Albanito, A. Madeo, R. Lappano, A. Vivacqua, V. Rago, A. Carpino, T. I. Oprea, E. R. Prossnitz, A. M. Musti, S. Ando, et al. G Protein-Coupled Receptor 30 (GPR30) Mediates Gene Expression Changes and Growth Response to 17{beta}-Estradiol and Selective GPR30 Ligand G-1 in Ovarian Cancer Cells Cancer Res., February 15, 2007; 67(4): 1859 - 1866. [Abstract] [Full Text] [PDF]
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N. Vasudevan and D. W. Pfaff Membrane-Initiated Actions of Estrogens in Neuroendocrinology: Emerging Principles Endocr. Rev., February 1, 2007; 28(1): 1 - 19. [Abstract] [Full Text] [PDF]
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P. Fan, J. Wang, R. J. Santen, and W. Yue Long-term Treatment with Tamoxifen Facilitates Translocation of Estrogen Receptor {alpha} out of the Nucleus and Enhances its Interaction with EGFR in MCF-7 Breast Cancer Cells Cancer Res., February 1, 2007; 67(3): 1352 - 1360. [Abstract] [Full Text] [PDF]
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K. Evaul, M. Jamnongjit, B. Bhagavath, and S. R. Hammes Testosterone and Progesterone Rapidly Attenuate Plasma Membrane G{beta}{gamma}-Mediated Signaling in Xenopus laevis Oocytes by Signaling through Classical Steroid Receptors Mol. Endocrinol., January 1, 2007; 21(1): 186 - 196. [Abstract] [Full Text] [PDF]
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S. Rice and S. A Whitehead Phytoestrogens and breast cancer -promoters or protectors? Endocr. Relat. Cancer, December 1, 2006; 13(4): 995 - 1015. [Abstract] [Full Text] [PDF]
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 X Li, V Rider, B F Kimler, and N I Abdou Estrogen does not regulate CD154 mRNA stability in systemic lupus erythematosus T cells Lupus, December 1, 2006; 15(12): 852 - 857. [Abstract] [PDF]
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T. Krietsch, M. S. Fernandes, J. Kero, R. Losel, M. Heyens, E. W.-F. Lam, I. Huhtaniemi, J. J. Brosens, and B. Gellersen Human Homologs of the Putative G Protein-Coupled Membrane Progestin Receptors (mPR{alpha}, {beta}, and {gamma}) Localize to the Endoplasmic Reticulum and Are Not Activated by Progesterone Mol. Endocrinol., December 1, 2006; 20(12): 3146 - 3164. [Abstract] [Full Text] [PDF]
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R. X-D Song, P. Fan, W. Yue, Y. Chen, and R. J Santen Role of receptor complexes in the extranuclear actions of estrogen receptor {alpha} in breast cancer Endocr. Relat. Cancer, December 1, 2006; 13(Supplement_1): S3 - S13. [Abstract] [Full Text] [PDF]
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 A. Vivacqua, D. Bonofiglio, L. Albanito, A. Madeo, V. Rago, A. Carpino, A. M. Musti, D. Picard, S. Ando, and M. Maggiolini 17beta-Estradiol, Genistein, and 4-Hydroxytamoxifen Induce the Proliferation of Thyroid Cancer Cells through the G Protein-Coupled Receptor GPR30 Mol. Pharmacol., October 1, 2006; 70(4): 1414 - 1423. [Abstract] [Full Text] [PDF]
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A. Pedram, M. Razandi, and E. R. Levin Nature of Functional Estrogen Receptors at the Plasma Membrane Mol. Endocrinol., September 1, 2006; 20(9): 1996 - 2009. [Abstract] [Full Text] [PDF]
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 L. Canesi, C. Ciacci, L. C. Lorusso, M. Betti, T. Guarnieri, S. Tavolari, and G. Gallo Immunomodulation by 17beta-estradiol in bivalve hemocytes Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2006; 291(3): R664 - R673. [Abstract] [Full Text] [PDF]
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Y. Zhu, L. L. Sullivan, S. S. Nair, C. C. Williams, A. K. Pandey, L. Marrero, R. K. Vadlamudi, and F. E. Jones Coregulation of Estrogen Receptor by ERBB4/HER4 Establishes a Growth-Promoting Autocrine Signal in Breast Tumor Cells Cancer Res., August 15, 2006; 66(16): 7991 - 7998. [Abstract] [Full Text] [PDF]
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J. E Sanchez-Criado, J. C Garrido-Gracia, C. Bellido, R. Aguilar, P. Guelmes, P. Abreu, R. Alonso, I. Barranco, Y. Millan, and J. M. de las Mulas Oestradiol-17{beta} inhibits tamoxifen-induced LHRH self-priming blocking hormone-dependent and ligand-independent activation of the gonadotrope progesterone receptor in the rat. J. Endocrinol., July 1, 2006; 190(1): 73 - 84. [Abstract] [Full Text] [PDF]
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R. X.-D. Song and R. J. Santen Membrane Initiated Estrogen Signaling in Breast Cancer Biol Reprod, July 1, 2006; 75(1): 9 - 16. [Abstract] [Full Text] [PDF]
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 R. J. Pietras Biologic Basis of Sequential and Combination Therapies for Hormone-Responsive Breast Cancer Oncologist, July 1, 2006; 11(7): 704 - 717. [Abstract] [Full Text] [PDF]
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M Marino, P Galluzzo, S Leone, F Acconcia, and P Ascenzi Nitric oxide impairs the 17{beta}-estradiol-induced apoptosis in human colon adenocarcinoma cells. Endocr. Relat. Cancer, June 1, 2006; 13(2): 559 - 569. [Abstract] [Full Text] [PDF]
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M. R. Meyer, E. Haas, and M. Barton Gender Differences of Cardiovascular Disease: New Perspectives for Estrogen Receptor Signaling Hypertension, June 1, 2006; 47(6): 1019 - 1026. [Full Text] [PDF]
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D.-b. Chen, S. Jia, A. G. King, A. Barker, S.-m. Li, E. Mata-Greenwood, J. Zheng, and R. R. Magness Global Protein Expression Profiling Underlines Reciprocal Regulation of Caveolin 1 and Endothelial Nitric Oxide Synthase Expression in Ovariectomized Sheep Uterine Artery by Estrogen/Progesterone Replacement Therapy Biol Reprod, May 1, 2006; 74(5): 832 - 838. [Abstract] [Full Text] [PDF]
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A. Pedram, M. Razandi, D. C. Wallace, and E. R. Levin Functional Estrogen Receptors in the Mitochondria of Breast Cancer Cells Mol. Biol. Cell, May 1, 2006; 17(5): 2125 - 2137. [Abstract] [Full Text] [PDF]
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 V. Vijayanathan, S. Venkiteswaran, S. K. Nair, A. Verma, T.J. Thomas, B. T. Zhu, and T. Thomas Physiologic levels of 2-methoxyestradiol interfere with nongenomic signaling of 17beta-estradiol in human breast cancer cells. Clin. Cancer Res., April 1, 2006; 12(7 Pt 1): 2038 - 2048. [Abstract] [Full Text] [PDF]
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A. E. Gururaj, S. K. Rayala, R. K. Vadlamudi, and R. Kumar Novel Mechanisms of Resistance to Endocrine Therapy: Genomic and Nongenomic Considerations Clin. Cancer Res., February 1, 2006; 12(3): 1001s - 1007s. [Abstract] [Full Text] [PDF]
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C. M. Bula, J. Huhtakangas, C. Olivera, J. E. Bishop, A. W. Norman, and H. L. Henry Presence of a Truncated Form of the Vitamin D Receptor (VDR) in a Strain of VDR-Knockout Mice Endocrinology, December 1, 2005; 146(12): 5581 - 5586. [Abstract] [Full Text] [PDF]
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D. D. Carson Uterine sensing of the embryo PNAS, June 14, 2005; 102(24): 8397 - 8398. [Full Text] [PDF]
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